Week 8 Renal Disorders PDF

WEEK 8: RENAL DISORDERS The Renal system Major role in homeostasis → filter 200 L of blood every 24 hours​ Approx. 1 L of filtered fluid converted → into urine and excreted per day​ Variety of dis. affect renal function by → inhibiting kidneys’ ability to regulate plasma v...

WEEK 8: RENAL DISORDERS The Renal system Major role in homeostasis → filter 200 L of blood every 24 hours​ Approx. 1 L of filtered fluid converted → into urine and excreted per day​ Variety of dis. affect renal function by → inhibiting kidneys’ ability to regulate plasma volume and osmolality​ Infection of kidneys or urinary tract is most common disorder affecting renal function​ Stones, tumors, inflammation, or consequences of medical procedures can→ obstruct and/or cause injury to the upper or lower urinary tract​ Renal system is directly linked to every other organ system​ Renal injury can affect other organs and become life-threatening!​ NEPHROLITHIASIS​(Kidney Stones/Renal Calculi) Nephrolithiasis: Risk Factors ○ Crystal, protein, or mineral salt form in urinary tract and may cause obstruction Most form in renal calyces (small chambers of the kidney where urine passes), renal pelvis, bladder Unilateral in about 80% of individuals Nephrolithiasis: Risk factors Age Seasonal factors Sex Fluid intake Race Diet Geographic location Occupation Genetic predisposition Kidney stone formation Supersaturation of one or more salts in urine ○ Salt has higher concentration than volume able to dissolve Precipitation of salts from liquid to solid state (crystals) ○ Temperature and PH Kidney stone → Growth via crystallization or agglomeration/to gather into a ball, mass, or cluster.  ○ Process → crystals grow from small nidus or nucleus → larger stones ○ Embedded in matrix Substances associated with stone formation ○ Hypercalciuria, Hyperoxaluria, hyperuricosuria, hypocitraturia, crystal growth inhibitor deficiencies ○ Alkaline urine PH → increases the risk of a calcium phosphate stone ○ Acidic urine PH → increases the risk of uric acid stone ○ Hyperparathyroidism and bone demineralization assosc. with prolonged immobilization → known to cause stone formation 4 Substances capable of inhibiting stone formation are (PPMT): Potassium citrate, Tamm-horsfall protein, pyrophosphate, magnesium ○ These reduce risk of calcium phosphate or calcium oxalate precip. in urine ○ Prevent → subsequent stone formation Stones are Classified According to the Primary Minerals (Salts)​ Composition of mineral salts: ○ Calcium oxalate and calcium phosphate (70% to 80%​) ○ Struvite (magnesium, ammonium, phosphate)​(1% to 5%​) ○ Uric acid​(5% to 10%​) Genetic disorders of amino acid metabolism​: ○ Excess urine can cause → cystinuric, xanthine, stone formation in presence of a low urine pH​ Definition: - Cystinuria (rare condition) is a stone made from amino acid called cysteine → form in the kidney, ureter, or bladder - Xanthine: a crystalline compound found in blood and urine, an intermediate in the metabolic breakdown of nucleic acids to uric acid. STONES NAMES & PICTURES: a. Calcium Oxalate and Calcium Phosphate: Idiopathic Hypercalciuria​ b. Calcium Oxalate and Calcium Phosphate: Hyperuricosuria​ c. Calcium Oxalate and Calcium Phosphate: Hyperoxaluria​ d. Magnesium-Ammonium-Phosphate (Struvite)​ e. Uric Acid: Anhydrous ​ f. Uric Acid: Dihydrate ± Uric Acid Anhydrous​ g. Cystine h. Unknown Classifications PICTURES BELOW: Stones Also Classified According to Location and Size!​(location & Size: Staghorn or Non-staghorn) Staghorn calculi ​ Large and fill the minor and major calyces​ Non-Staghorn calculi​ Variable size and smaller​ Located in calyces, renal pelvis, different places along ureter​ Evaluation and Diagnosis of Kidney Stones​ Presenting symptoms​ ○ Renal colic (pain)​→ How would one describe renal colic and what other signs and symptoms History​ ○ Dietary habits​ ○ Age of first stone episode​ ○ Stone analysis​ ○ Presence of complicating factors​ Focused physical assessment​ Imaging studies​ ○ Location of stone, severity of obstruction, associated obstructive uropathy​ Urinalysis (including pH) ​ 24-hour urine​ Retrieve and analyze stones​ Additional tests completed ​ ○ With suspected hyperparathyroidism (elevated serum calcium levels)​ ○ With cystine calculi, or uric acid (high purine diet) stones​ Tx of Kidney Stones Managing pain Reducing the concentration of stone forming substances  Adjusting the ph of urine Decreasing the amount of stone-forming substances Removing stones using percutaneous nephrolithotomy, , ureteroscopy, or ultrasonic or laser lithotripsy to fragment stones for excretion​ - Emergency!! → Obstructing kidney stones with suspected proximal UTI are urologic emergencies → requiring emergent decompression, stone removal, and antibiotics!​ - What health teaching would you provide to your client about how to prevent recurrent kidney stones?​__________________________________________________________ PYELONEPHRITIS & GLOMERULONEPHRITIS Acute Pyelonephritis Acute Pyelonephritis: Infection of one or both upper urinary tracts​, one or both kidneys may be involved​ Common Causes​ Nephrolithiasis, pregnancy, neurogenic bladder, instrumentation, female sex trauma​ Acute infection of ureter, renal pelvis, and/or kidney interstitium​ Most common underlying risk factors: Urinary obstruction and reflux of urine from bladder (vesicoureteral reflux) Risk Factors for Acute Pyelonephritis​ ➔ Premature newborns​ ➔ Prepubertal children​ ➔ Sexually active and pregnant women​ ➔ Women treated with antibiotics that disrupt vaginal flora​ ➔ Spermicide users​ ➔ Estrogen-deficient postmenopausal women​ ➔ Individuals with​ ◆ Indwelling catheters​ ◆ Diabetes​ ◆ Neurogenic bladder​ ◆ Urinary tract obstruction​ Acute Pyelonephritis: Pathophysiology​ E. coli (most common), Proteus, or Pseudomonas​ Microorganisms also split urea into ammonia→ making an alkaline urine → increases risk of stone formation​ Infection spread by ascending uropathic microorganisms​ May also spread through blood​  Inflammatory process affects kidney pelvis, calyces, medulla​ ○ Infiltration of leukocytes with renal inflammation, renal edema, purulent urine​ In severe infections​ ○ Abscesses may form in medulla and extend to cortex​ Tubules primarily affected, while glomeruli usually spared​ ○ After acute phase, healing occurs with fibrosis and atrophy of affected tubules​ Necrosis of renal papillae can develop​ Manifestations of Acute Pyelonephritis​ Onset of symptoms is usually acute: ○ Fever, chills ○ Tachycardia ○ Nausea, vomiting ○ Flank/groin pain ○ UTI symptoms Older adults ○ Early nonspecific symptoms i.e low grade fever ○ Confusion malaise Evaluation and Treatment of Acute Pyelonephritis​ Evaluation and diagnosis ○ Established by urine culture, urinalysis, clinical manifestations Urine culture assay establishes definitive diagnosis though identification of uropathogen White blood cell casts Treatment ○ Antibiotic administration How do UTIS cause pyelonephritis - Bacteria from gut flora → urinary tract inflammation f the urinary epithelium → retrograde/moving backward of bacteria into urethra bladder → ureter → kidney → can lead to pyelonephritis, inflammation of upper urinary tract PHARMACOTHERAPY FOR ACUTE PYELONEPHRITIS​ Ciprofloxacin​(Antibiotics for Uncomplicated Acute Pyelonephritis): Classification: Fluoroquinolones​ Drug: Ciprofloxacin ​ Indication: Uncomplicated Acute Pyelonephritis​ Mechanism of Action:​ Ciprofloxacin inhibits two bacterial enzymes: DNA gyrase and topoisomerase IV.​ These enzymes are critical for bacterial DNA synthesis and replication.​ Desired Effect: Bactericidal action against gram-negative bacteria​ Adverse Effects:​ Common: Nausea, vomiting, and diarrhea​ Serious: Dysrhythmias, liver failure​ CNS effects: Dizziness, headache, sleep disturbances​ Antacids, ferrous sulfate, and sucralfate decrease absorption – What is the nursing implication? ​ Trimethoprim-Sulfamethoxazole (TMP-SMX)​(Antibiotics for Uncomplicated Acute Pyelonephritis): Classification: Sulfonamides​ Indication: Uncomplicated Acute Pyelonephritis​ Mechanism of Action:​ TMP-SMX is a combination of two drugs, trimethoprim, and sulfamethoxazole​ They inhibit sequential steps in bacterial folic acid synthesis, essential for bacterial growth and replication​ Desired Effect: Bactericidal action against gram-negative bacteria​ ​Adverse Effects:​ Common: Nausea, vomiting, rash​ Serious: Stevens-Johnson syndrome, blood disorders ​ Additional considerations for ciprofloxacin and trimethoprim-sulfamethoxazole​ Fluoroquinolones (Ciprofloxacin):​ Well absorbed orally, ideal for outpatient therapy​ Safety profile: Monitor for dysrhythmias, liver function, and CNS effects​ Caution in children (potential impact on cartilage development)​ Avoid use in pregnant or lactating clients​ First-line drug for post-exposure prophylaxis to Bacillus anthracis (anthrax)​ Sulfonamides (TMP-SMX):​ Take with plenty of water to prevent crystalluria​ Caution in clients with allergies, Stevens-Johnson syndrome risk​  Avoid in pregnancy and breastfeeding​ Potential for blood disorders, monitor closely​ Gentamycin​ Classification: Aminoglycosides (bactericidal antibiotic)​ Indication: Severe or Complicated Acute Pyelonephritis​ Mechanism of Action:​ It inhibits bacterial protein synthesis and causes the synthesis of abnormal proteins​ Desired Effect: Treatment of severe infections with aerobic gram-negative bacteria, mycobacteria, and some protozoans​ Adverse Effects:​ Ototoxicity: May cause hearing loss and balance disturbances​ Nephrotoxicity: May cause kidney injury.​ Neuromuscular blockade: Risk of muscle weakness and apnea​ Interactions: Risk of nephrotoxicity increases with concurrent use of other nephrotoxic drugs​ note: Increased risk of ototoxicity with amphotericin B, furosemide, aspirin, cisplatin, and others​ How would the nurse monitor for adverse effects: ______________________________________________________________________________ Acute Glomerulonephritis ​ Inflammation isolated to kidney glomerulus​is caused by primary glomerular injury ○ Infection, immunologic responses, ischemia, free radicals, drugs, toxins, vascular disorders​ Secondary glomerular injury​ Glomerular injury occurring as consequence of systemic diseases, including:​ ○ Diabetes, hypertension, bacterial toxins, systemic lupus erythematosus, congestive heart failure, HIV-related kidney disease​ Injury to Glomerulus​ ○ Immune glomerular injury​ Most common is antigen-antibody complexes depositing in glomerular capillary wall or mesangium​ Immunoglobulin A (IgA) nephropathy​ ○ Nonimmune glomerular injury​ Injury or ischemia from metabolic disorders, toxin exposure, drugs, vascular disorders, infection​ Immunologic Pathogenesis of Glomerulonephritis​ Injury begins after antigen-antibody complexes are formed​ Immune injury caused by activation of inflammatory response!​  ○ Complement activation, leukocyte recruitment, release of cytokines from leukocytes​ Complement deposited with the antibodies​ ○ Complement activation can cause cell injury or attract leukocytes (neutrophils, monocytes, T lymphocytes) through chemotactic stimulus ​ Phagocytes and activated platelets increase inflammatory reaction!​ ○ Release mediators that injure glomerular filtration membrane including epithelial cells, glomerular basement membrane, and endothelial cells (podocytes and filtration slits)​ Injury increases glomerular filtration membrane permeability and reduces glomerular membrane surface area​ Hypertrophy and proliferation of mesangial cells and expansion of extracellular matrix in Bowman space​ ○ Deposition of these substances and cell proliferation forms a crescent shape within Bowman space​ ○ Crescent formation is associated with rapidly progressive glomerulonephritis​ Result of these processes is ​ ○ Compression of glomerular capillaries, decreased glomerular blood flow, hypoxic injury, decreased driving glomerular hydrostatic pressure, alteration in filtration membrane, and decreased GFR​ Loss of normal negative electrical charge across glomerular filtration membrane and increase in filtration pore size enhance movement of proteins and red blood cells into urine​ ○ Proteinuria and/or hematuria develop​ Severity of glomerular damage and decline in glomerular function is related to​ ○ Size, number, and location of cells injured ​ Focal: affecting some glomeruli​ Diffuse: affecting glomeruli throughout kidney​ Duration of exposure​ Type of antigen-antibody complexes formed​ Mechanisms of Glomerular Injury: The BIG Picture! ​ Inflammation of glomerulus ​ Antibodies produced against organism that cross-react with glomerular endothelial cells ​ Activation of complement​ Recruitment and activation of immune cells and mediators​ Decreased glomerular filtration rate (GFR)​ Decreased glomerular perfusion (glomerular blood flow) as a result of inflammation​ ○ Glomerular sclerosis (scarring)​  ○ Thickening of glomerular basement membrane, but increased permeability to proteins and red blood cells​ ​Acute Glomerulonephritis: Manifestations​ May be silent, mild, moderate, or severe in symptom presentation!​ Severe or rapidly progressive glomerulonephritis​ Hematuria with red blood cell casts​ Smoky, brown-tinged urine​ Proteinuria exceeding 3–5 g/day with albumin​ Macroalbuminuria​ Low serum albumin​ Edema​ Oliguria​ Urine output 30 mL/hour or less​ Hypertension​  Renal failure​ Acute Glomerulonephritis: Evaluation and Diagnosis​ ○ Urinalysis​ Proteinuria, red blood cells, white blood cells, casts​ ○ Reduced GFR​ Elevated plasma urea, cystatin C, and creatinine concentrations, or reduced renal creatinine clearance​ ○ Renal biopsy ​ Determines renal injury and location and character of glomerular lesions ​ ○ Electron microscopy​ Morphologic changes within glomerular capillary wall​ ○ Staining with fluorescein​ Identifies complement and different antibodies and associated configurations ​ ○ Microscopy​ Provides information about distribution and lesions of immune response injury​ Guides therapy​ Acute Glomerulonephritis: Management and Treatment​ Management principles for treating glomerulonephritis related to ​ Treating primary cause​ Preventing or minimizing immune responses​ Correcting accompanying problems​ Edema, hypertension, hypoalbuminemia, hyperlipidemia​ Specific treatment regimens are necessary for particular types of glomerulonephritis​ (What would each of these drugs/treatments be used for? WHY would you anticipate that they may be ordered?​) Antibiotics​ Corticosteroids​ Cytotoxic agents​ Anticoagulants​ Diuretics or dialysis​ PHARMACOTHERAPY FOR ACUTE GLOMERULONEPHRITIS​ Treatment of Acute Glomerulonephritis: ​Penicillin Classification: Antibacterial drugs​ Indication: Treatment of various bacterial infections, including pneumonia, meningitis, skin and soft tissue infections, and certain genitourinary tract infections​  Mechanism of Action: Disrupting the cell walls of bacteria, leading to their death. Target the penicillin-binding proteins in the bacterial cell wall, weakening it and causing cell lysis​ Desired Effects​ Eradication of the bacterial infection causing acute glomerulonephritis​ Reduction of inflammation and immune response to protect glomerular function​ Resolution of clinical manifestations and abnormal laboratory findings associated with glomerular disease​ Adverse Effects​ Allergic reactions, including anaphylaxis (most common)​ Diarrhea, nausea, and vomiting​ Superinfections, including antibiotic-associated pseudomembranous colitis (AAPMC), may develop.​ In some cases, renal impairment may occur due to the accumulation of penicillins in clients with compromised kidney function​ Corticosteroids​ a. glucocorticoid b. Mineralocorticoid Systemic glucocorticoids Wide therapeutic application​ Short-term use due to potentially serious adverse effects​ Suppress histamine release and inhibit the synthesis of prostaglandins by COX-2; inhibit the immune system by suppressing certain functions of phagocytes and lymphocytes reduce inflammation​ Serious adverse effects: suppression of the normal functions of the adrenal gland (adrenal insufficiency), hyperglycemia, mood changes, cataracts, peptic ulcers, electrolyte imbalances, and osteoporosis; mask infections​ ​Prednisone​ Classification: Synthetic glucocorticoid​ Indications for use: anti-inflammatory (short-term); maintain adrenal function (long-term)​ Mechanisms of Action: decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation​ Desired effects: prevent inflammation, reduce risk of bronchospasm in patients with asthma or certain cancers; immunosuppressive at higher dose​ Adverse effects: Cushing’s syndrome (long-term), fluid retention​ What are some nursing implications:_______________________________________________________ Renal disorders in children - Incidence and type of renal disorders experienced by children vary with age and maturation​ - Newborn disorders may involve congenital malformations​ - During childhood, kidney and genitourinary structures are continuing to develop, so renal dysfunction may be associated with mechanisms and manifestations that are different from those in adults​ Glomerular Disorders in Children​ Most common glomerular disorders in children are​ - Acute post-streptococcal glomerulonephritis​ - Immunoglobulin A nephropathy​ - Nephrotic syndrome​ - Hemolytic uremic syndrome​ Most glomerular diseases are acquired and immunologically mediated!​ Acute Poststreptococcal Glomerulonephritis​ ○ Most common in children ages 5 to 12 years and uncommon in children before age of 3 years​ Major cause of morbidity with hemolytic Streptococcal infections​ ○ Occurs after throat or skin infection with certain strains of Streptococcus pyrogenes (hemolytic Streptococcus) ​ Antigen-antibody complexes deposited in glomerulus​ Immune complexes initiate inflammation and glomerular injury​ Complex activates complement and release of inflammatory mediators that recruit neutrophils and macrophages and damages endothelial and epithelial cells in glomerular basement membrane​ Damage to glomerular basement membrane alters membrane permeability and leads to hematuria and proteinuria​ Acute Poststreptococcal Glomerulonephritis: Manifestations and Treatment​ Symptoms begin 1 to 2 weeks after an upper respiratory tract infection ​ ○ Pharyngitis, more common during cold weather​ Symptoms begin up to 6 weeks after a skin infection​ ○ Impetigo, more common during warm weather​ Clinical manifestations​ ○ Sudden onset of hematuria, proteinuria, renal insufficiency, edema, hypertension​ ○ Oliguria may be present​  ○ Headache, vomiting, somnolence, other CNS manifestations​ ○ Dyspnea, tachypnea, and enlarged tender liver ​ Treatment​ ○ Supportive and symptom-specific​ ○ Antibiotic therapy​ ○ Restrict fluid, sodium, potassium intakes​ ○ Administer antihypertensive drugs​ ○ Administer diuretics​ Immunoglobulin A (IgA) Nephropathy​ Most common form of glomerulonephritis in children​ Deposition of IgA immune complexes with activation of complement​ Initiates inflammatory response in mesangium of glomerulus​ Recurrent microscopic or gross hematuria concurrent with respiratory tract infection (i.e., tonsillitis) or gastroenteritis​ Most continue to have microscopic hematuria between attacks of gross hematuria and have a mild proteinuria​ Supportive treatment, dialysis, transplantation​ Immunoglobulin A Vasculitis: Henoch-Schönlein Purpura Nephritis​ ​Rare form of IgA nephropathy​ But, most common form of systemic vasculitis in children​ ○ Immune-mediated immunoglobulin A (IgA) vasculitis​ Causes inflammation and damage to glomerular blood vessels​ ○ Clinical manifestations​ Palpable purpura​ Arthralgia​ Abdominal pain​ Renal disease​ Hematuria and/or proteinuria​ Treatment​ ○ Most children recover with supportive care​ ○ Some progress to end stage renal disease (kidney failure)​ ○ Severe symptoms require administration of steroids and other immunosuppressant drugs​ ○ ACEIs​ Hemolytic Uremic Syndrome​ Acute disorder characterized by hemolytic anemia, thrombocytopenia, and acute renal failure​ Considered a thrombotic microangiopathy ​  Most common community-acquired cause of acute kidney injury in children​ Occurs mostly in those younger than 4 years of age​ What Causes Hemolytic Uremic Syndrome?​ Bacterial and viral agents​ Also endotoxins, i.e. Shiga toxin-producing Escherichia coli (diarrhea associated hemolytic uremic syndrome, D+)​ Potential sources of exposure include:​ - Animals, unpasteurized beverages, undercooked meat, and vegetables​ Genetic forms (nondiarrhea or atypical) are rare ​ - Caused by other microorganisms or by inherited abnormality in complement alternate pathway regulation (i.e., von Willebrand factor–cleaving protease)​ - Major characteristic is absence of prodromal diarrhea, thus designation D−​ Hemolytic Uremic Syndrome (D+): Pathophysiology​ Verotoxin from E. coli absorbed from intestine into blood​ ○ Binds to white blood cells which are transported to kidney​ In kidney, white blood cells cause damage to glomerular endothelium​ ○ With activation of coagulation cascade and aggregation of platelets​ Glomerular arterioles become swollen and occluded with platelets and fibrin clots​ ○ Causes decreased glomerular filtration rate with hematuria and proteinuria​ Swollen and narrowed glomerular vessels damage passing red blood cells and platelets​ ○ Damaged red blood cells and platelets removed by spleen, causing acute hemolytic anemia and thrombocytopenia​ Fibrinolysis acts on precipitated fibrin​ Varying degrees of renal vascular occlusion cause altered renal perfusion and renal insufficiency or failure!​ Hemolytic Uremic Syndrome: Triad​ Hemolytic anemia​ Thrombocytopenia​ Renal insufficiency​ Hemolytic Uremic Syndrome: Manifestations​ Prodromal GI illness​ ○ Diarrhea with or without vomiting precedes onset by 1 to 2 weeks​ After symptom-free 1- to 5-day period​ ○ Sudden onset of pallor, bruising or purpura, irritability, weakness, oliguria​ Accompanying symptoms​ ○ Slight fever, anorexia, vomiting, diarrhea (stool characteristically watery and blood stained), abdominal pain, mild jaundice, circulatory overload ​ Seizures and lethargy​  ○ CNS involvement​ Severe cases​ ○ Renal failure within first days of onset​ Renal failure causes metabolic acidosis, azotemia (accumulated nitrogenous wastes in the blood), hyperkalemia, hypertension​ Hemolytic Uremic Syndrome: Evaluation​ ​Clinical evaluation includes​ History of preexisting illness​ Presenting symptoms​ Urine analysis​ Blood analysis ​ Hemolytic Uremic Syndrome: Treatment​ Maintain nutrition​ Maintain hydration (to dilute toxins)​ Control hypertension, hyperkalemia, seizures​ Fluid and electrolyte management​ Blood transfusions with packed red cells​ ○ Maintain reasonable hemoglobin levels​ Dialysis support during acute phase​ Most children recover completely, but potential long-term sequelae include​ ○ Renal (hypertension, proteinuria, chronic kidney disease, end stage renal disease)​ ○ Nonrenal abnormalities (diabetes, neurologic manifestations)​